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(undergrad) physiology > 2 week 12 > Flashcards

2 week 12 Flashcards

1
Q

functions of blood? (5)

A
  • transports gases, nutrients, hormones, metabolic wastes.
  • regulates composition of interstitial fluid.
  • restricts fluid loss at injury sites via blood clotting.
  • defends against toxins and pathogens.
  • regulates body temp by absorbing and redistributing heat.
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1
Q

what are the constituents of blood?

A
  • plasma: 55%
  • erythrocytes: 45%
  • buffy coat (WBC + platelets): less than 1%
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2
Q

what is plasma made of?

A
  • 92% water
  • ions, organic molecules, trace elements, gases
  • organic molecules = proteins like albumins (60%), globulins (36%), fibrinogen (4%)
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3
Q

where are most plasma proteins made? and does plasma have a greater or lesser concentration of proteins than interstitial fluid?

A
  • liver
  • greater
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4
Q

where do blood cells and platelets come from? what is this process called?

A
  • stem cells
  • hematopoiesis
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5
Q

main function of erythrocytes? how do they obtain their energy?

A
  • transport oxygen and contain carbonic anhydrase needed for transport of carbon dioxide.
  • no nucleus or organelles… obtain energy via glycolysis
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6
Q

describe the structure of a hemoglobin molecule

A
  • identical alpha and beta subunits
  • 4 heme groups (meaning it can bind 4 oxygens)
  • iron in centre of heme group; non-covalent
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7
Q

what is hematocrit? average for males vs females?

A
  • ratio of erythrocytes : total blood volume (centrifuged sample)
  • males: 40-54
  • females: 37-47
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8
Q

what is polycythemia? why can this be dangerous?

A
  • adaptive response; higher hematocrit in low-oxygen environments.
  • i.e., ppl living at high altitudes can have 60 hematocrit.
  • dangerous because makes blood have high viscosity = clots.
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9
Q

describe the life cycle of erythrocytes (6)

A
  • formation = erythropoiesis (in red bone marrow)
  • stimulated by erythropoietin (released from kidney in response to low oxygen)
  • no cell division of mature RBCs
  • short life span = 120 days
  • replace 2–3 million RBCs/second
  • old RBCs filtered by spleen (and liver)
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10
Q

which portion of the RBC is eliminated? where does it go?

A
  • heme!
  • converted to bilirubin and excreted
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11
Q

what is…
a) aplastic anemia
b) nutritional anemia
c) pernicious anemia
d) renal anemia

A

a) drugs destroy stem cells
b) inadequate iron, folic acid, vitamin b12
c) deficiency in intrinsic factor like GI tract
d) kidney failure = low erythropoietin

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12
Q

what causes anemia? (5)

A
  • genetics
  • parasitic infections
  • drugs
  • autoimmune reactions (hemolytic)
  • excessive blood loss (hemorrhagic)
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13
Q

what are the 4 blood types we discussed and what are the differences among them?

A
  • A: has A antigens and antiB antibodies [42%]
  • B: has B antigens and antiA antibodies [9%]
  • AB: has A and B antigens; no antibodies (universal recipient!) [3%]
  • O: has no antigens and antiA and antiB antibodies (universal donor!) [46%]
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14
Q

what is the main function of WBC? what is its structure like? (3)

A
  • immune system
  • nucleated
  • several types
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15
Q

types of WBC and their functions? (5)

A
  • neutrophils: phagocytes that circulate in blood for 7-10hrs and numbers increase during infections [50-80%].
  • lymphocytes: B become plasma cells that produce antibodies, T activate immune cells and kill abnormal cells, and so do natural killers [20-40%].
  • monocytes: migrate to tissues and become macrophages which phagocytose bacteria, present antigens to T cells and secrete cytokines [2-8%].
  • eosinophils: defend against parasites via toxic granules [1-4%].
  • basophils: defend against larger parasites and release histamine and heparin [<1%].
16
Q

what is hemostasis? its 3 phases?

A
  • stopping bleeding from a broken vessel.
  • phases = 1) vascular spasm, 2) platelet plug formation, 3) clotting/coagulation.
17
Q

describe the 3 phases in more depth

A

1) vascular spasm: injury = vasoconstriction thx to sympa system… reduces blood flow but does not stop bleeding.

2) platelet plug formation: von Willebrand factor (vWf) is secreted by platelets/endothelial cells + binds to collagen to activate platelets which form around site of vessel damage. platelets also release TXA2 and ADP!

3) clotting/coagulation: clot forms within plug to support it. does so by converting fibrinogen to fibrin (see common pathway slide).

18
Q

where do platelets come from?

A
  • break off into fragments from multinucleated megakaryocyte
  • thrombopoietin produces megakaryocytes
  • platelets themselves are anucleated but DO contain organelles
19
Q

what do undamaged cells do to inhibit platelet aggregation?

A

endothelial cells release prostacyclin

20
Q

describe the common pathway

A
  • inactive 10 cleaved to 10a
  • 10a, 5, calcium ions, and PF3 cleave inactive prothrombin into active thrombin
  • thrombin cleaves fibrinogen to form fibrin mesh network (cleaved by 13a, to get stable mesh network)
21
Q

describe extrinsic pathway

A

inactive 3 + inactive 7 + calcium form “active7 complex” that cleaves inactive 10 into 10a

22
Q

describe intrinsic pathway

A
  • inactive12 + collagen = active12
  • active 12 cleaves inactive11 = active11
  • active11 works with calcium to cleave inactive9 = active9
  • active 9 works with 8 + calcium + PF3 to cleave inactive10 = active10!
23
Q

what dissolves the clot when its no longer needed?

A

plasmin (activated by TPA)

24
Q

thrombus vs embolus?

A
  • thrombus: attaches to vessel wall
  • embolus: free floating clot
25
Q

what are hemophilia A and B?

A
  • delay in formation of fibrin
  • A = defective factor 8
  • B = defective factor 9
26
Q

what is thrombocytopenia? what do thrombocytopenia, vitamin K deficiency, and vWf disease have in common?

A
  • thrombocytopenia = low platelet count
  • all 3 = interference with platelet adhesion to collagen
27
Q

treatment for vWf disease?

A

desmopressin to increase vWf levels

28
Q

preventions/treatments for excessive clotting? (3)

A
  1. heparin: prevents thrombin activity
  2. warfarin/coumadin: prevents clotting (by suppressing vitamin K)
  3. aspirin: prevents TXA2 synthesis (prevents plug formation)

(undergrad) physiology (21 decks)

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